A continuation of a study into the mechanism(s) of increased intraocular pressure induced by topical administration of glucocorticoids is proposed. In addition, the effect of cortisol on the lens will be studied in order to determine a possible mechanism for cataract formation associated with the pharmacological use of glucocorticoids. We will identify which of the specific cells of the ciliary epithelium bind glucocorticoids and study the nuclear translocation of the steroid-receptor complex and its role in inducing the synthesis of specific RNA and proteins. These will be done in primary cultures from the human and the rabbit and when available in stable cell lines derived from these tissues. The trabecular meshwork from glaucomatous eyes will be examined by immunofluorescent staining for several proteins which may be implicated in the decreased outflow facility associated with primary open angle glaucoma. The study of peripheral lymphocyte receptors will be concluded. The metabolism of glucocorticoids and the role of these steroids in cellular differentiation of the lens will be initiated.